Download HYPERTENSIVE HEART DISEASE Hypertensive heart disease

HYPERTENSIVE HEART DISEASE
Hypertensive heart disease (HHD) stems from the increased
demands placed on the heart by hypertension pressure overload
+ ventricular hypertrophy
Most commonly seen in the left heart systemic hypertension
Pulmonary hypertension  right-sided HHD / cor pulmonale.
SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE
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Hypertrophy of the heart is an adaptive response
– Pressure overload can cause:
– Myocardial dysfunction,
– Cardiac dilation,
– CHF,
– Sudden death.
THE MINIMAL CRITERIA FOR THE DIAGNOSIS OF SYSTEMIC
HHD:
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left ventricular hypertrophy (usually concentric) in the
absence of other cardiovascular pathology
A history or pathologic evidence of hypertension.
The Framingham Study established unequivocally that even
mild hypertension (levels only slightly above 140/90 mm Hg),
if sufficiently prolonged, induces left ventricular hypertrophy.
Appr 25% of the population of the United States suffers from
hypertension
MORPHOLOGY.
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Hypertension induces left ventricular pressure overload
hypertrophy
Initially without ventricular dilation
Left ventricular wall thickening increases the weight of the heart
disproportionately to the increase in overall cardiac size
The thickness of the left ventricular wall may exceed 2.0 cm
Heart weight may exceed 500 gm.
Increased thickness of the left ventricular wall imparts a
stiffness that impairs diastolic fillingleft atrial enlargement.
MICROSCOPICALLY
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The earliest change of systemic HHD is an increase in the
transverse diameter of myocytes, which may be difficult to
appreciate on routine microscopy.
At a more advanced stage variable degrees of cellular and
nuclear enlargement become apparent, often accompanied by
interstitial fibrosis.
The biochemical, molecular, and morphologic changes that
occur in hypertensive hypertrophy are similar to those noted in
other conditions associated with myocardial pressure overload.
PULMONARY (RIGHT-SIDED) HYPERTENSIVE
HEART DISEASE (COR PULMONALE)
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Cor pulmonale, as isolated pulmonary HHD is
frequently called, stems from pressure overload of
the right ventricle
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Characterized by:
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Right ventricular hypertrophy,
Dilation,
Failure secondary to pulmonary hypertension.
Disorders of the lungs, especially chronic respiratory
diseases such as emphysema, or primary pulmonary
hypertension.
PH is most frequently associated with structural
cardiopulmonary conditions that increase pulmonary blood flow
or pressure (or both), pulmonary vascular resistance, or left
heart resistance to blood flow
These include the following:
CHRONIC OBSTRUCTIVE OR INTERSTITIAL LUNG
DISEASES:
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Patients with these diseases have hypoxia as well as
destruction of lung parenchyma and hence have fewer alveolar
capillaries. This causes increased pulmonary arterial
resistance and, secondarily, elevated pressure.
ANTECEDENT CONGENITAL OR ACQUIRED HEART
DISEASE:
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PH occurs in patients with mitral stenosis, for example,
because of an increase in left atrial pressure that leads to an
increase in pulmonary venous pressure and, consequently, to
an increase in pulmonary artery pressure.
Recurrent Thromboemboli:
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Patients with recurrent pulmonary emboli may have PH
primarily due to a reduction in the functional cross-sectional
area of the pulmonary vascular bed brought about by the
obstructing emboli, which, in turn, leads to an increase in
pulmonary vascular resistance.
CONNECTIVE TISSUE DISEASES:
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Several of these diseases (most notably systemic sclerosis)
involve the pulmonary vasculature, leading to inflammation,
intimal fibrosis, medial hypertrophy, and PH.
OBSTRUCTIVE SLEEP APNEA
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A common disorder that is associated with obesity and is now
recognized to be a significant contributor to the development of
pulmonary hypertension and cor pulmonate.
DISEASES OF THE PULMONARY PARENCHYMA
• Chronic obstructive pulmonary disease
• Diffuse pulmonary interstitial fibrosis
• Pneumoconioses
• Cystic fibrosis
• Bronchiectasis
DISEASES OF THE PULMONARY VESSELS
• Recurrent pulmonary thromboembolism
• Primary pulmonary hypertension
• Extensive pulmonary arteritis (e.g., Wegener granulomatosis)
• Drug-, toxin-, or radiation-induced vascular obstruction
• Extensive pulmonary tumor microembolism
DISORDERS AFFECTING CHEST MOVEMENT
• Kyphoscoliosis
• Marked obesity (sleep apnea, pickwickian syndrome)
• Neuromuscular diseases
DISORDERS INDUCING PULMONARY ARTERIAL CONSTRICTION
• Metabolic acidosis
• Hypoxemia
• Chronic altitude sickness
• Obstruction of major airways
• Idiopathic alveolar hypoventilation
MORPHOLOGY
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In acute cor pulmonale there is marked dilation of the right
ventricle without hypertrophy.
On cross-section the normal crescent shape of the right
ventricle is transformed to a dilated ovoid.
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In chronic cor pulmonale the right ventricular wall thickens,
sometimes up to 1.0 cm or more
More subtle right ventricular hypertrophy may take the form of
thickening of the muscle bundles in the outflow tract,
immediately below the pulmonary valve, or thickening of the
moderator band, the muscle bundle that connects the
ventricular septum to the anterior right ventricular papillary
muscle.
Sometimes, the hypertrophied right ventricle compresses the
left ventricular chamber, or leads to regurgitation and fibrous
thickening of the tricuspid valve.
Normally, the myocytes of the right ventricle are haphazardly
arranged and the wall contains transmural fat; in right
ventricular hypertrophy, fat in the wall disappears and the
myocytes align themselves circumferentially.
CLINICAL COURSE.
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Idiopathic PH is most common in women who are 20 to 40
years of age
Dyspnea
Fatigue
Chest pain of the anginal type.
Severe respiratory distress,
Cyanosis
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Right ventricular hypertrophy
Death from decompensated cor pulmonale
REFERANCES
ROBBINS BASIC PATHOLOGY
8th EDITION
Pg =198 – 199
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